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Clinical Pharmacology and Therapeutics > Drugs Used in Neurological Disorders > Flashcards

Drugs Used in Neurological Disorders Flashcards

1
Q

What main 2 neurological disroders can we treat?

A

Idiopathic parkinson’s disease

Myasthenia Gravis

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2
Q

What is the pathophysiology of IPD?

A

Neurodegeneration in the substantia nigra in the cells which produce dopamine, leading to reduced number of dopaminergic neurones

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3
Q

How are catecholamines synthesised?

A

L-tyrosine -> L-DOPA -> Dopamine -> Norepinepherine/NA -> Epinepherine (adrenaline)

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4
Q

How is L-tyrosine converted to L-DOPA?

A

By tyrosine hydroxylase

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5
Q

How is L-DOPA converted to dopamine?

A

By DOPA decarboxylase

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6
Q

How is dopamine converted to NA?

A

By dopamine B-hydroxylase

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7
Q

What 2 enzymes can break down dopamine?

A

COMT then MAO/aldehyde dehydrogenase

MAO/aldehyde dehydrogenase then COMT

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8
Q

What is the end product of dopamine breakdown?

A

Homovanillic acid

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9
Q

What are the 3 ways to manage IPD?

A

Treat symptoms, neuroprotection, and surgery

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10
Q

What should be offered to pts with early IPD to manage motor symptoms (which decrease QoL)?

A

Levodopa

combined with carbidopa (co-careldopa) or benserazide (co-beneldopa)

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11
Q

If IPD pts aren’t affected (QoL) by motor symptoms, which drugs can pts be offered?

A

Levodopa
Dopamine receptor agonists
MAO-B inhibitors

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12
Q

How does levodopa work?

A

Formulation of L-DOPA that crosses the blood brain barrier and is taken up by dopaminergic cells in the SN where it -> dopamine

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13
Q

What is the disadvantage of levodopa?

A

If there are fewer SN cells (more progressed disease), its effect is lessened as it cannot be converted

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14
Q

How is levodopa administered?

A

Orally

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15
Q

Describe what happens in absorption of levodopa

A

Levodopa is absorbed in the gut by active transport (competition with amino acids).
90% is inactivated in the intestinal wall by MAO and dopa decarboxylase

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16
Q

What is the half life of levodopa?

A

2 hours

17
Q

What does this half life mean for levodopa dosage and effect?

A

Short dose interval so blood levels can fluctuate, so symptoms also fluctuate

18
Q

How much levodopa is converted to dopamine in peripheral tissues?

A

9%

19
Q

What does this peripheral conversion of levodopa mean, practically?

A

It can cause peripheral tissue side effects, such as hypertension

20
Q

What does the remaining 1% of levodopa compete with to get across the BBB?

A

Amino acids again

21
Q

How can levodopa administration and effect be maximised?

A

Different formulations with a DOPA decarboxylase inhibitor

22
Q

What are the 2 formulations of levodopa with dopa decarboxylase inhiitors?

A

Co-careldopa (sinemet)

Co-beneldopa (madopar)

23
Q

How much L-DOPA reaches the brain in levodopa cobined formulations?

A

About 10%

24
Q

What are the advantages of levodopa?

A

Very effective

Low side effects

25
Q

What ADRs can be experienced with levodopa?

A

Nausea/anorexia
Hypotension
Psychosis
Tachycardia

26
Q

What are the disadvantages of levodopa?

A

Needs enzymatic conversion
Loss of efficacy long term
Involuntary movements and motor complications

27
Q

What can increase the breakdown of levodopa?

A

Pyroxidine/Vit B12 (breakdown in peripheries)

28
Q

What is a risk with levodopa and MAO inhibitors together?

A

Hypertensive crisis

29
Q

Which group of drugs block dopamine receptors?

A

Antipsychotics

30
Q

What 4 groups of dopamine receptor agonists are there?

A

Ergot derived (not used)
Non-ergot derived
Patch
Subcut

31
Q

What types of non ergot dopamine receptor agonists are there?

A

Ropinirole

Pramipexole

32
Q

What dopamine receptor agonist patch is there?

A

Rotigotine

33
Q

What subcut dopamine receptor agonist is there?

A

apomorphine

Clinical Pharmacology and Therapeutics (26 decks)

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